Butin inhibits osteoarthritis progression by modulating the Nrf2/HO-1 signaling pathway and inhibiting NF-κB signaling

The current treatment of osteoarthritis is limited to the reliever treatment of anti-inflammatory drugs, and there is still a lack of safe and effective drug treatment. Butin, a flavonoid, has the potential to be a drug candidate due to its excellent anti-inflammatory and antioxidant effects. However, the molecular mechanism of Butin's anti-inflammatory and antioxidant mechanisms is still unclear, so in this study, we explored Butin's role in alleviating osteoarthritis and the role of Butin in regulating the Nrf2/HO1/NF-κB axis of cellular antioxidant defense. We used the MTT test, the EdU test, and flow cytometry (FCM) to validate Butin's effect on IL-1β-induced chondrocyte cell viability. Western blot (WB) was used to detect the Nrf2/HO1/NF-κB axis-related proteins to explore the effect of Butin on the Nrf2/HO1/NF-κB axis. In addition, we used quantitative real-time polymerase chain reaction (qPCR), Elisa, flow cytometry to detect cartilage extracellular matrix characteristic proteins (Aggrecan, Collagen II, MMP13 and ADAMTS5). The results showed that Butin could effectively up-regulate the Nrf2/HO1 axis, reduce NF-κB expression, improve chondrocyte damage, and alleviate the progression of osteoarthritis.